OBJECTIVE: To evaluate the effect of clonidine on the experimental neuropathic pain model and to observe whether neuropathic pain is related to the sympathetic nervous system in this model by reversal of allodynia with administration of epinephrine. METHOD: The neuropathic pain was produced by unilateral transection of the superior caudal trunk innervating the rat's tail. Tail withdrawal responses based on mechanical (withdrawal frequency to bending force of von Frey hair 2.0 g) and the thermal (withdrawal latency to tail immersion in a 4degrees C or 40degrees C water with a cut-off time of 15 seconds) stimuli were used. Experiments were performed two weeks after surgery when neuropathic pain had fully been developed. Experimental group by administration of clonidine was examined by tail withdrawal responses at Day 1, Day 3 and Day 5. After one week of wash-out period, reversal of allodynia by administration of epinephrine was examined by the same test. RESULTS: Clonidine significantly decreased the frequency of withdrawal with the mechanical stimuli compared with control (P<0.01), but did not significantly decrease with the cold or warm stimuli. Epinephrine tended to aggravate the mechanical allodynia, but it was not significant compared with the control. CONCLUSION: Clonidine may relieve mechanical allodynia in neuropathic pain, but the mechanism of neuropathic pain that is related to the sympathetic nervous system in this experimental model may be unreliable.